Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway

Figure 1 Impaired viability of islet β-cells in acute pancreatitis models. A-F: Cell Counting Kit-8 assay was used to assess the proliferation of islet β-cells (MIN-6) under control conditions, lipopolysaccharide stimulation (5 μg/mL or 10 μg/mL), and co-culture with media from lipopolysaccharide-treated 266-6 cells (A). Apoptosis in islet β-cells was evaluated in both acute pancreatitis cell and mouse models using the terminal deoxynucleotidyl transferase dUTP nick-end labeling assay (B and E). Quantitative analysis of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive β-cells (C and F). Insulin secretion by islet β-cells in the acute pancreatitis model was quantified with an enzyme-linked immunosorbent assay kit (D). Representative results from three independent replicates are shown (n = 8). ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001. Data are presented as the mean ± SD. LPS: Lipopolysaccharide; AP: Acute pancreatitis; MAP: Mild acute pancreatitis; SAP: Severe acute pancreatitis; HE: Hematoxylin and eosin.